Medical Nutrition Therapy in

Cardiovascular Disease
 PROSES METABOLISME
NUTRIEN OKSIGEN

INTAKE KEBUTUHAN PANKREAS

INSULIN
GLUKAGON

SAL. CERNA SAL. NAFAS

HATI

CO2
SAL. KARDIOVASKULER

KULIT GINJAL
SEL-SEL TUBUH
METABOLISME:
KATABOLISME UREA N
AIR & PANAS ANABOLISME KREATININ
AIR & ELEKTROLIT
A Nation at Risk
49 million Americans smoke
42 million have total cholesterols
>240 mg/dl
63 million have total cholesterols
200-239
17 million Americans have diabetes
61 million Americans are obese; 68
million are overweight
Framingham
Milestones
1960: cigarette smoking found to
increase the risk of heart disease
1961: Cholesterol level, blood
pressure, and EKG abnormalities found
to increase the risk of heart disease
1967: physical activity found to reduce
the risk of heart disease; obesity found
to increase the risk of heart disease
1970: High blood pressure found to
increase the risk of stroke
Framingham
Milestones
1976: Menopause found to increase
the risk of heart disease
1978: Psychosocial issues found to
affect the risk of heart disease
1988: High levels of HDL found to
reduce risk of death
1994: Enlarged left ventricle found to
increase the risk of stroke
1996: Progression from hypertension
to heart failure described
Coronary Heart Disease
(CHD) or Coronary Artery
Disease
(CAD)impeded blood flow to
Disease involves
the network of blood vessels surrounding
and serving the heart
Major cause is atherosclerosis; structural
and compositional changes in the inner
wall of the arteries
Manifested in clinical end points of
myocardial infarction (MI) and sudden
death
Pathophysiology of
Atherosclerosis
Vessel lining is injured (often at
branch points)
Plaque is deposited to repair
injured area
Plaque thickens, incorporating
cholesterol, protein, muscle cells,
and calcium (rate depends partly
on level of LDL-C in the blood)
Pathophysiology of
Atherosclerosis (cont)
Arteries harden and narrow as
plaque builds, making them less
elastic
Increasing pressure causes
further damage
A clot or spasm closes the
opening, causing a heart attack
Pathophysiology of
Atherosclerosis
Proliferation of smooth-muscle
cells, macrophages, and
lymphocytes
Formation of smooth muscle cells
into a connective tissue matrix
Accumulation of lipid and
cholesterol in the matrix around
the cells
Endothelial Injury
Caused by
Hypercholesterolemia
Oxidized low-density lipoprotein
Hypertension
Cigarette smoking
Diabetes
Obesity
Homocysteine
Diets high in saturated fat and cholesterol
Natural Progression of
Atherosclerosis

(From Harkreader H. Fundamentals. Philadelphia: W.B. Saunders, 2000)

Heart Attack
(Myocardial Infarction)
Heart Attack
(Myocardial Infarction)
When blood supply to the heart is
disrupted, the heart is damaged
May cause the heart to beat
irregularly or stop altogether
25% of people do not survive
their first heart attack
Symptoms of a Heart
Attack
Intense, prolonged chest pain or
pressure
Shortness of breath
Sweating
Nausea and vomiting
(especially women)
Dizziness (especially women)
Weakness
Jaw, neck and shoulder pain
(especially women)
Irregular heartbeat
Factors That May Bring
On Heart Attack (in at-
risk)
Dehydration
Emotional stress
Strenuous physical activity when
not physically fit
Waking during the night or
getting up in the morning
Eating a large, high-fat meal
(increases risk of clotting)
Cerebrovascular
Accident (CVA) or
Brain Attack
Brain Attack (Stroke)
or Cerebrovascular
Accident
Functions of
Lipoproteins
Lipids are transported in the blood bound
to protein
Lipoproteins vary in composition, size, and
density
Consist of varying amounts of triglyceride,
cholesterol, phospholipid, and protein
The ratio of protein to fat determines the
density (HDLs have more protein than
LDLs)
Lipoproteins combine

Lipids (triglycerides,
cholesterol)
Protein

Phospholipids
Functions of the
Plasma Lipoproteins
ChylomicronTransport of dietary
triglyceride
VLDLTransport of endogenous
triglyceride
IDLLDL precursor
LDLMajor cholesterol transport
lipoprotein
HDLReverse cholesterol transport
Lipoprotein Summary
Lipoprotein
Assessment
Includes measurement of total
cholesterol, LDL cholesterol, HDL
cholesterol, and triglyceride level
after fasting
Total Cholesterol
Captures cholesterol contained in all
lipoprotein fractions
60%-70% is carried on LDL
20%-30% is carried on HDL
10%-15% on VLDL
Total Cholesterol
Direct, positive association between TC
and CHD risk
Diets high in saturated fats raise total
cholesterol and CHD incidence and
mortality
ATP-III Guidelines: lowering total
cholesterol and LDL-C reduces CHD risk
10% reduction in TC decreases CHD risk
by about 30%
Factors Affecting Total
Cholesterol
Age Drugs (beta
Diets high in fat, blockers, thiazide
saturated fat, diuretics)
cholesterol Body weight
Genetics Glucose tolerance
Endogenous sex Physical activity
hormones (pre- Season of the year
menopause)
Diseases
Exogenous steroids
Total Triglycerides
Triglyceride-rich lipoproteins include
chylomicrons, VLDL, remnants or
intermediary products
Are atherogenic
At very high levels, risk of
pancreatitis
Can be evidence of metabolic
syndrome
Chylomicrons
Largest particles
Transport dietary fat and cholesterol
from the small intestine to the liver
In the bloodstream, triglycerides are
hydrolyzed by lipoprotein lipase (LPL)
in muscle and adipose tissue
When 90% of triglyceride is
hydrolyzed, released into blood as a
remnant
Liver metabolizes remnants, but some
deliver cholesterol to the arterial wall
Absent in fasting studies
Very-Low-Density-
Lipoproteins
Manufactured in the liver to transport
endogenous triglyceride and
cholesterol
60% is triglyceride
Large VLDL may be nonatherogenic
VLDL remnants or IDL appear to be
atherogenic
Not routinely measured, but TG in
them is measured in total triglyceride
Intermediate-Density
Lipoprotein
Formed with catabolism of VLDL, a
precursor of LDL
Rich in cholesterol and apo E
High concentrations of IDL and VLDL
remnants directly related to lesion
progression and coronary events
Not routinely measured, though
components can be
Low-Density
Lipoprotein
Primary cholesterol carrier in blood
Total cholesterol and LDL-cholesterol
are strongly correlated
95% of apolipoproteins in LDL are apo-
B-100
LDL is formed in VLDL catabolism, 60%
is taken up by LDL receptors in liver,
adrenals, other tissues; rest is
metabolized via alternative pathways
Number and activity of receptors
determines LDL cholesterol levels in the
blood
 LDL-C
Particles heterogeneous in size, density,
lipid components
Phenotype A: large particles, not associated
with disease risk
Phenotype B typified by small, dense LDL
particles; triglyceride rich, cholesterol
depleted; predictive of
CHD risk in men and women
High Density
Lipoproteins (HDL)
Contain more protein than
the other lipoproteins
Apo A-1 is involved in
tissue cholesterol removal
High HDL is associated with
low levels of chylomicrons,
VLDL remnants, and small,
dense LDL
Lipoprotein Profile
Measures total cholesterol, LDL-
cholesterol, HDL-cholesterol, and
triglycerides
8-12 hour fast allows chylomicrons
to clear
Friedenwald formula for calculating
LDL-C = (TC) (HDL-C) (TG/5)
Lipoprotein Profile
If nonfasting, can measure total
and HDL cholesterol
If TC>200 mg/dl or HDL-C is <40
mg/dl, get fasting analysis
 Evaluating Blood
Lipids: Total
Cholesterol
<200 mg/dL Desirable

200-239 Borderline high

mg/dL

240 mg/dL High

Source: ATP-III Guidelines, NHLBI, accessed 2-2005

 Evaluating Blood
Lipids: Triglycerides
<150 mg/dL Normal

150-199 Borderline high

200-499 High

>500 mg/dl Very high

Source: ATP-III Guidelines, NHLBI, accessed 4-2005

 Evaluating Blood
Lipids: LDL
<100 mg/dL Optimal

100-129 Near optimal

130-159 Borderline high

160-189 High

190 Very high

Source: ATP-III Guidelines, NHLBI, accessed 2-2005

Evaluating Blood
Lipids: HDL
< 40 mg/dL Low

60 mg/dL High

Source: ATP-III Guidelines, NHLBI, accessed 2-2005

Risk Factors affect
Lipid Targets
Major, independent risk factors
Life-habit risk factors
Emerging risk factors
 Major Risk Factors That
Modify LDL Goals
Cigarette smoking
Hypertension (BP 140/90 mmHg or
on
antihypertensive medication)
Low HDL cholesterol (<40 mg/dL)
Family history of premature CHD
CHD in male first degree relative <55
CHD in female first degree relative <65
Age (men 45 years; women 55

years)
Life-Habit Risk Factors
Obesity (BMI 30)
Physical inactivity
Atherogenic diet
Emerging Risk Factors
Lipoprotein (a)
Homocysteine
Prothrombotic factors
Proinflammatory factors
Impaired fasting glucose
Subclinical atherosclerosis
Risk Assessment
Count major risk factors*
For patients with multiple (2+) risk factors
Perform 10-year risk assessment
For patients with 01 risk factor
10 year risk assessment not required
Most patients have 10-year risk <10%

*HDL cholesterol 60 mg/dL counts as a negative risk

factor; its presence removes one risk factor from the total
count.
CHD Risk Equivalents

Risk for major coronary events

equal to that in established CHD
10-year risk for hard CHD >20%

Hard CHD = myocardial infarction + coronary

death
Diabetes

In ATP III, diabetes is

regarded
as a CHD risk equivalent.
Diabetes as a CHD Risk
Equivalent
10-year risk for CHD 20%
High mortality with established
CHD
High mortality with acute MI
High mortality post acute MI
CHD Risk Equivalents
Other clinical forms of
atherosclerotic disease (peripheral
arterial disease, abdominal aortic
aneurysm, and symptomatic carotid
artery disease)
Diabetes
Multiple risk factors that confer a
10-year risk for CHD >20%
Calculate Your 10-Year
Risk of Heart Attack
Risk Calculation
http://hp2010.nhlbihin.net/atpiii/
calculator.asp?usertype=pub
At-A-Glance treatment guidelines:

http://www.nhlbi.nih.gov/guideline
s/cholesterol/atglance.htm
 Three Categories of
Risk that Modify LDL-C
GOALS
Risk Category LDL Goal
(mg/dL)
CHD and CHD risk
equivalents
<100
Multiple (2+) risk
factors
<130
Zero to one risk
factor <160
ATP III Guidelines

Goals and Treatment

Overview
Primary Prevention
With
LDL-Lowering Therapy
Public Health Approach
Reduced intakes of saturated fat
and cholesterol
Increased physical activity
Weight control
Causes of Secondary
Dyslipidemia
Diabetes
Hypothyroidism
Obstructive liver disease
Chronic renal failure
Drugs that raise LDL cholesterol and
lower HDL cholesterol (progestins,
anabolic steroids, and
corticosteroids)
 Secondary Prevention
W/
LDL-Lowering Therapy
Benefits: reduction in total mortality,
coronary mortality, major coronary
events, coronary procedures, and stroke
LDL cholesterol goal: <100 mg/dL
Includes CHD risk equivalents
Consider initiation of therapy during
hospitalization
(if LDL 100 mg/dL)
LDL-C Goals in Different Risk
Categories
LDL for Total LDL for
Lifestyle Drug Therapy
LDL Goal Change (TLC)
Risk Category
(mg/dL) (mg/dL) (mg/dL)
CHD or CHD
<100; 100
Risk
optional (<100:
Equivalents 100
goal <70 consider drug
(10-year risk
mg/dL options
>20%)
Moderately
high risk >130 mg/dL
(100-129
2+ Risk <130 130 mg/dL,
Factors consider drug
(10-year risk options)
10-20%)

ATP-3 update, Circulation, 2004

LDL-C Goals in
Different Risk
Categories LDL for Total
LDL for
Lifestyle
Drug Therapy
LDL Goal Change (TLC)
Risk Category (mg/dL)
(mg/dL) (mg/dL)

Moderate risk: <130 mg/dL >130 mg/dL >160 mg/dL

2+ risk factors
(10 year
risk<10%)

Lower risk (0- <160 mg/dL >160 mg/dL >190 mg/dL

1 risk factors) (160-189
mg/dL, drug
optional)

ATP-3 update, Circulation, 2004

Congestive Heart
Failure (CHF)
A clinical syndrome characterized
by progressive deterioration of
left ventricular function,
inadequate tissue perfusion,
fatigue, shortness of breath, and
congestion
Congestive Heart Failure (CHF)
contd
Gradual failure of heart
1. CompensatedLack of O2 to
tissues causes increase in heart
rate and enlargement of heart
2. DecompensatedHeart no
longer adjusts
Causes of Heart
Failure
Diseases of the heart (valves, muscle,
vessels, arteries) and vasculature
(hypertension) cause left ventricular
systolic dysfunction
Once established, myocardial infarction,
dietary sodium excess, medication
noncompliance, arrhythmias, pulmonary
embolism, infection, anemia can
precipitate complete CHF
Risk Factors
Hypertension (91% of Framingham
cohort had hypertension before CHF)
Left ventricular hypertrophy
Coronary heart disease (causes 60-
65% of cases)
Diabetes
Mean age of onset is 70 years
Stages of Heart Failure
A High risk of HF HBP, CAD, diabetes, alcohol
because of presence abuse, hx rheumatic fever;
of risk factors but family hx cardiomyopathy,
without syx or using cardiotoxins, metabolic
structural damage syndrome

B Structural heart LVH or fibrosis, left ventricular

disease associated dilatation; low EF;
with HF but no asymptomatic valve disease,
signs/syx previous MI

C Structural heart Dyspnea or fatigue due to LV

disease with current dysfunction; reduced exercise
or prior syx of HF tolerance
D Advanced structural Frequently hospitalized;
damage, refractoryth awaiting transplant
Krummel in Krause, 12 Ed.
symptoms
Classifications of Heart
Failure
Class I No undue symptoms associated
with ordinary activity; no
limitations
Class II Slight limitation of physical
activity; patient comfortable at
rest
Class Marked limitation of physical
III activity; patient comfortable at
rest
Class Inability to carry out physical
Congestive Heart Failure
Symptoms
Dyspnea
Orthopnea
Nausea
Fullness
Pulmonary edema
Cardiac edema
Cardiac cachexia
CHF DIAGNOSIS
EKG or electrocardiogram
measures the rate and regularity of
the heartbeat
May indicate whether there has been
heart damage or changes in anatomy
Chest X-ray
Shows whether heart is enlarged,
fluid in lungs, pulmonary disease
CHF DIAGNOSIS
Echocardiogram
Most useful test in diagnosis of heart
failure
Uses sound waves to create a
picture of the heart
Evaluates heart function: cardiac
output and areas of the heart that
are not contracting normally
Other Cardiac Tests
Holter Monitor: ambulatory
electrocardiography
Worn for 24 hours and provides a continuing
recording of heart rhythm during normal
activity
Cardiac Blood Pool Scan (radionuclide
ventriculography or nuclear scan)
Uses radioactive imaging agent injected
into a vein to outline chambers of the heart
and blood vessels
Shows how well heart is pumping blood to
the rest of the body
Other Cardiac Tests
Cardiac Catheterization
Flexible tube passed through vein in the
groin or arm to reach the coronary arteries
Allows physician to visualize the arteries,
check pressure and blood flow in coronary
arteries, collect blood samples
Coronary angiography: usually done
along with cardiac catheterization
Dye injected into coronary arteries and/or
chambers of the heart
Allows angiographer to visualize flow of
blood
Cardiac Tests
Exercise Stress Test
EKG and blood pressure readings are
taken before, during, and after
exercise to determine how the heart
responds to exercise
Patient exercises on a treadmill or
stationary bike until reaches a
heartrate established by the physician
Echocardiogram often included
BNP and NT-proBNP
Blood Test
Measure the concentration of BNP
(hormone made by the heart) or NT-
proBNP (both formed when pro-BNP is
cleaved into two fragments)
Released as a natural response to
heart failure, to hypotension, and to
LVH
Used to grade the severity of heart
failure
Cachectic Heart
A soft, flabby heart characterized
by loss of myocardial mass as
the result of extreme
malnutrition
Congestive Heart
Failure
Goal: decrease work of heart
Treatment
Diet
1. Na restriction (500 to 1000 mg)
2. Monitor serum Khypokalemia possible
with diuretics and digoxin)
3. Fluid restriction
4. Alcoholnone to moderate
5. Caffeinecan cause MI or cardiac
arrhythmia
Medications Used in
Heart Failure
Diuretics help reduce fluid buildup in lungs and
peripheral edema
ACE inhibitors lower blood pressure and reduce
the strain on the heart. These medications also
may reduce the risk of a future heart attack.
Beta blockers slow heart rate and lower blood
pressure to decrease the workload on the heart.
Digoxin makes the heart beat stronger and pump
more blood.
Vasodilators: reduce blood pressure and stress on
the heart
MNT in HF
Fluid restriction
Sodium restriction
Meet energy/protein needs
Prevent cardiac cachexia
Small frequent meals
Fluid Restriction
If hyponatremia occurs (serum
sodium <130 mEq/L)
Limit total fluids to <2000 ml
In severe decompensation, limit to
1000-1500 ml
Maintain restricted sodium diet even
if serum sodium depleted; sodium
has moved from blood to tissues
Fluid Status and
Assessment
Patients should record daily
weights and advise care providers
if weight gain exceeds 2-3 lb a
day or 5 lb in a week
Restricting sodium and fluids
(decreasing by 1 to 1.5 cups) may
prevent complete HF
Fluid Calculations
Hospitalized patients may be
limited to 500-2000 ml daily
Foods having a high fluid content
may also be limited
Foods that are liquid at room
temperature such as ice cream,
yogurt, gelatin, popsicles count
towards fluid allotment
Living with Fluid
Restrictions
Freezing fruit or sucking on sugar
free hard candy may help
Fluid status monitored by measuring
urine specific gravity and serum
electrolyte values and observing for
clinical signs of edema
Restrictions often discontinued when
patients leave the hospital
Cardiac Cachexia
Involuntary weight loss of >6% of
nonedematous body weight over a 6-
month period
Significant loss of lean body mass:
exacerbates HF
Cachectic heart: soft and flabby
Structural, circulatory, metabolic,
inflammatory, and neuroendocrine
changes in skeletal muscle
Serious complication of HF
Cardiac Cachexia
Patients with cardiac cachexia may lose
10-15% of their body weight (dry weight)
Other markers (serum prealbumin and
transferrin) may be disproportionately
low because of the dilutional effect of
excess fluid
Use anthropometrics (measurement of
calf and thigh circumference, MUAC) and
diet history
Cardiac Cachexia
Proinflammatory state in which cytokines
(TNF, IL-1 and I-6) are elevated in the
blood and myocardial tissue
Reduced blood flow to the gut may
reduce gut integrity leading to entry of
bacteria and endotoxins
High TNF associated with reduced BMI,
lower skinfolds, reduced visceral proteins

Krummel in Krause, 12th ed., 2008

Energy Needs in HF
For obese patients, hypocaloric diets
(1000-1200 kcals) will reduce the
stress on the heart
In undernourished patient, energy
needs are increased by 30-50% above
basal levels; 35 kcals/kg often used
Patients with cardiac cachexia may
require 1.6-1.8 times resting energy
expenditure for repletion
Sodium
Impaired cardiac function inadequate
blood flow to the kidneys aldosterone
and antidiuretic hormone secretion
Aldosterone promotes sodium resorption
and ADH promotes water conservation
Even patients with mild heart failure can
retain sodium and water if consuming a
high salt diet (6 g or 250 mEq/day)
Sodium in Patients with

Heart Failure
Recommendations vary between
1200 to 2400 mg/day (adequate
intake 1200 mg/d)
Patients on high dose lasix (>80
mg/day) <2000 mg
Severe restrictions are unpalatable
and nutritionally inadequate
Ethnic differences in sodium intake
Use least restrictive diet that
achieves clinical goals
Dietary Sources of
Sodium
Salt used at the table
Salt or sodium compounds added during
preparation or processing
Inherent sodium in foods
Chemically softened water
Average American consumes 4 to 6 g
sodium/day; 80% from processed foods
Minimum to maintain life is 250 mg/day
Salt substitutes, herbs, spices and other
seasonings
Drugs and antacids may contain sodium
Characteristics of
Common Sodium
Restrictions
3 g (131 mEq) High sodium foods are limited; no more
No added salt than t of table salt allowed

2 g (87 mEq) High sodium foods are eliminated;

Mild restriction moderate sodium foods are limited; no
more than t of table salt allowed
1 g (43 mEq) High and moderate sodium foods
Moderate eliminated; table salt not allowed;
canned/processed foods containing salt
omitted; frozen peas, lima beans,
mixed veg and corn omitted d/t brine in
processing; regular bread and baked
goods limited. Difficult to maintain at
home
500 mg Sodium Diet
High sodium, moderate sodium foods eliminated.
Table salt not allowed. Canned or processed
foods containing salt omitted
Frozen vegetables (peas, lima beans, mixed
vegetables, corn) omitted due to brine
High sodium vegetables beets, beet greens,
carrots, kale, spinach, celery, white turnips,
rutabagas, mustard greens, chard, dandelion
greens omitted
Low sodium bread instead of regular bread
Meat limited to 6 ounces
 Food Labeling Guide
(standard serving)
Sodium Free Less than 5 mg
Very Low Sodium 35 mg or less
Low Sodium 140 mg or less
Reduced Sodium At least 25% less sodium
than regular food
Light Sodium 50% less sodium
Unsalted, No salt added during
processing Without Added Salt,
No Salt Added
Lightly Salted 50% less added sodium than
normally added (product must
state not a low-sodium food)
Nondietary Sources of
Sodium
Medications: barbiturates,
sulfonamides, antibiotics, cough
medications, stomach alkalizers,
laxatives, mouthwashes
Chewable antacid tablet can add
1200 to 7000 mg of sodium daily
Aspirin: 50 mg sodium per tablet
Potassium
Potassium wasting diuretics
(hydrochlorthiazide, furosemide) increase
potassium excretion which may lead to
digitalis toxicity
Some patients will need potassium
supplements
Salt substitutes can provide 500-2000 mg
of potassium per teaspoon; contraindicated
in renal failure and with certain other
medications
Sodium and Salt Gram
and Milliequivalent
Measures

1 mEq Na = 23 mg NA
Other Dietary Factors
in
Heart Failure
Alcohol and caffeine
Weight maintenance
Calcium and vitamin D
Magnesium
Thiamin supplementation
Small frequent feedings
Supplements
Other Nutritional
Issues
Calcium and Vitamin D: half of patients
with severe HF have osteopenia or
osteoporosis, especially cachectic
patients; use calcium supplements
with caution w/ cardiac arrhythmias
Magnesium: diuretics may increase mg
excretion; measure blood mg levels
Thiamin status should be evaluated in
HF patients on loop diuretics
Cardiac Assist Devices
Mechanical heart pumps
May be helpful in pre-transplant
HF patients or in those for whom
transplant is not an option